The principal objectives are to investigate those host responses which result in the various immunopathologic lesions seen in schistosomiasis mansoni, and to attempt to thwart such lesion formation by alteration of the immune status of the host. The main area of interest will focus upon schistosome egg granuloma formation. Investigations will be undertaken to establish the pathogenesis of aberrent granuloma formation in T lymphocyte-depleted or congenitally athymic mice. These studies will scrutinize the role of immune-complexes, toxic products, anatomical locations, and complete infection, in this situation. Furthermore, studies will be continued on immune interactions that lead to modulation of granuloma formation during chronic disease. These investigations will analyse the roles of enhancing antibodies, suppressor T lymphocytes, "null set" lymphocytes, and the participation of various accessory cell types. This study will be aided by a parallel investigation which will be aimed at reproducing granuloma formation in an in vitro system. This model should allow the addition or deletion of the various reactants presumed to be important in this process, and thereby allow dissection of the roles of these components. Such studies will continue to concentrate on eosinophil functions and interrelationships, and then expand to encompass other cell types and soluble mediators. Another area to be examined concerns the potential role of immunosuppressive effects exerted during schistosomiasis. This will initially by investigated in relationship to the development of the toxemic, or acute, Katayama fever syndrome.